Effect of acetate on palmitate oxidation in bovine and rat skeletal muscle tissue

We postulated that the low rate of long-chain fatty acid (LCFA) oxidation in ruminant tissues is attributable to inhibition by high concentrations of acetate normally present in ruminants. Gastrocnemius muscle was excised from rats (n=14) after euthanasia and from lactating Holstein cows either by surgical biopsy (n=9) or after slaughter (n=2). Muscle slices (20-100 mg) were incubated for 60 min at 37°C in Ca-free Krebs-Ringer bicarbonate buffer (pH 7.4) containing 0.5 or 2.0 mM [1-¹⁴C]palmitate complexed to bovine serum albumin (4:1 molar ratio). Flasks also contained 0, 0.5 or 2.0 mM sodium acetate. ¹⁴CO₂ was collected and quantified by liquid scintillation. Bovine muscle oxidized less (P<.005)palmitate than rat muscle (3.55 vs. 20.07 nmol/h·g wet tissue in the absence of acetate). In bovine muscle, acetate suppressed (P<.05) oxidation of 2.0 mM palmitate (by 34.3% and 35.7% for 0.5 and 2.0 mM acetate) but did not affect oxidation of 0.5 mM palmitate. In rat muscle, acetate suppressed (P<.05) oxidation of 0.5 mM palmitate (by 49.1% and 49.2% for 0.5 and 2.0 mM acetate) but did not affect oxidation of 2.0 mM palmitate. Muscle slices also were incubated with [1-¹⁴C]acetate without or with palmitate (rat n = 10, cow n= 9). Bovine muscle oxidized less (P<.0001) acetate man rat muscle (60.85 vs. 239.47 nmol/h·g wet tissue in the absence of palmitate). Palmitate did not affect acetate oxidation in bovine muscle. In rat muscle, palmitate (2.0 mM) suppressed (P<.05) oxidation of 0.5 mM acetate by 69.0%. These data are consistent with the hypothesis that greater in vivo concentrations of acetate in ruminants contribute to lower rates of LCFA oxidation by ruminant muscle.